摘要
本实验以肺希夫氏硷(Schiff base)做为检测自由基致伤指标,观察了大鼠烟雾吸入后12小时内肺希夫氏硷和肺损伤变化情况。同时观察了耗竭白细胞对大鼠伤后肺希夫氏硷的影响,主要结果为:1.肺希夫氏硷伤后30分钟和6小时分别高于对照组56.2%(P<0.01)和31.4%(P<0.01)。说明自由基参与了吸入性损伤的致伤过程。2.耗竭白细胞伤后30分钟组和8小时组肺希夫氏硷分别下降了33.7%(P<0.05)和50.3%(P<0.05),提示白细胞为自由基的一个重要来源,其作用在伤后6小时尤为突出。
In this study,lung Schiff Base was used as a measure indicating the lung injury induced by free radicals, and lung water, lung vascular permeability, blood gases levels as well as pulmonary pathomorphological change (JM) as measures denoting extents of lung injury after inhalation injury. Experiment was Perfonmed on ats ard cbserved for a period of 12 hr post smoke inhalation. In addition, control studies were also achieved on normal rats,and rats depleted from leukocytes by cyclophosphamide prior to the experiments. The results were, 1. The lung Schiff bases Were generally higher than that of the control through the whole observation period and two peaks were demonstrated at 30'and 6 hr(56.2% and 31.4% higher than controls respectively) indicating that free radicals played a significant role on lung damage in smoke inhalation injury. 2. Lung Schiff bases of rats depleted from leukocytes revealed a 33.7% and a 50.3% reduction respectively at 30' and 6 hr after injury. It seems that leukoeytes lead a more important position at 6 hr than at 30' after injury. 3. The reduction rates of peripheral leukocytes, lung Sehiff bases and lung water content were not identical in rats depleted from leukocyte after inhalation injury. There were 94.3%, 50.3% and 42.6% reducticn respectively at 6 hr after injury. Correlations among them were not significant. These data suggest that after smoke inhalation injury leukocyte is not the only source of free radicals and also the free radicals are not the only means which leukocyte rely upon to cause lung injury.
